This study is the first to link potential mechanisms between OSA and prolonged QTc and SCD, suggesting an inverse association with mRNA expression of K+ channels with severity of OSA. CPAP therapy diminishing OSA is able to reverse this relationship in 4&nbsp;weeks for moderate OSA. It remains to be determined whether this effect persists in the long term and what duration of therapy is required to restore circulating levels to those in subjects without OSA. Studies showing reproducibility and an association with measured QTc levels during sleep and wakefulness will strengthen this observation. Also requiring clarification is the nature of the interaction between K+ channel remodeling and hypoxemia and other acute effects of apnea, in the genesis of QT prolongation during apneas.

Mentions:
OSA is also associated with increased VE activity of 60% when compared to subjects without OSA (4% to 12%), which can be decreased with the use of OSA therapies.10 VEs initiating VA in prolonged QTc, especially during severe hypoxemia, may be key mechanisms for SCD in OSA (Figure 2). Potentiating mechanisms may include hemodynamic instability, increased platelet aggregation, plaque disruption and release of vasoactive substances, inflammation, oxidative stress, endothelial dysfunction, and thrombosis. Direct mechanisms include the effects of a Mueller maneuver (repetitive forced inspiration against a closed upper airway) with substantial negative intrathoracic pressures, which can increase transvalvular gradients, wall stress, and afterload, which can be proarrhythmogenic. This can also increase the risk for aortic dissection and rupture, resulting in SCD. Other possible effects include altering cardiac cellular electrophysiology with prolongation of QT interval, during which the heart is susceptible to VA initiation.

Mentions:
OSA is also associated with increased VE activity of 60% when compared to subjects without OSA (4% to 12%), which can be decreased with the use of OSA therapies.10 VEs initiating VA in prolonged QTc, especially during severe hypoxemia, may be key mechanisms for SCD in OSA (Figure 2). Potentiating mechanisms may include hemodynamic instability, increased platelet aggregation, plaque disruption and release of vasoactive substances, inflammation, oxidative stress, endothelial dysfunction, and thrombosis. Direct mechanisms include the effects of a Mueller maneuver (repetitive forced inspiration against a closed upper airway) with substantial negative intrathoracic pressures, which can increase transvalvular gradients, wall stress, and afterload, which can be proarrhythmogenic. This can also increase the risk for aortic dissection and rupture, resulting in SCD. Other possible effects include altering cardiac cellular electrophysiology with prolongation of QT interval, during which the heart is susceptible to VA initiation.

This study is the first to link potential mechanisms between OSA and prolonged QTc and SCD, suggesting an inverse association with mRNA expression of K+ channels with severity of OSA. CPAP therapy diminishing OSA is able to reverse this relationship in 4&nbsp;weeks for moderate OSA. It remains to be determined whether this effect persists in the long term and what duration of therapy is required to restore circulating levels to those in subjects without OSA. Studies showing reproducibility and an association with measured QTc levels during sleep and wakefulness will strengthen this observation. Also requiring clarification is the nature of the interaction between K+ channel remodeling and hypoxemia and other acute effects of apnea, in the genesis of QT prolongation during apneas.